ArticleEnvironmental health perspectives2011
Genetic variation in base excision repair pathway genes, pesticide exposure, and prostate cancer risk.
Article in Environmental health perspectives, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 46 citations in OpenAlex.
- Research progress on the role of the NEIL family in cancer.Frontiers in cell and developmental biology · 2025Review
- Transcription Factor MAZ Potentiates the Upregulated NEIL3-mediated Aerobic Glycolysis, thereby Promoting Angiogenesis in Hepatocellular Carcinoma.Current cancer drug targets · 2024Article
- Joint associations between established genetic susceptibility loci, pesticide exposures, and risk of prostate cancer.Environmental research · 2023Article
- Construction of Bone Metastasis-Specific Regulation Network Based on Prognostic Stemness-Related Signatures in Prostate Cancer.Disease markers · 2022Article
- Article
- Occupational Risk Factors for Prostate Cancer: A Meta-analysis.Journal of cancer prevention · 2019Review
- TDG Gene Polymorphisms and Their Possible Association with Colorectal Cancer: A Case Control Study.Journal of oncology · 2019Article
- Functional Polymorphisms in DNA Repair Genes Are Associated with Sporadic Colorectal Cancer Susceptibility and Clinical Outcome.International journal of molecular sciences · 2018Article
- Sex Steroid Hormone Single-Nucleotide Polymorphisms, Pesticide Use, and the Risk of Prostate Cancer: A Nested Case-Control Study within the Agricultural Health Study.Frontiers in oncology · 2016Article
- EDC-2: The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals.Endocrine reviews · 2015Review
- Systematic evaluation of underlying defects in DNA repair as an approach to case-only assessment of familial prostate cancer.Oncotarget · 2015Article
- Requiring pollutant discharge permits for pesticide applications that deposit residues in surface waters.International journal of environmental research and public health · 2014Article
- Interactions between urinary 4-tert-octylphenol levels and metabolism enzyme gene variants on idiopathic male infertility.PloS one · 2013Article
- Genetic variation in the base excision repair pathway, environmental risk factors, and colorectal adenoma risk.PloS one · 2013Article
- Genetic variation in nucleotide excision repair pathway genes, pesticide exposure and prostate cancer risk.Carcinogenesis · 2012Article
- The Interaction between Pesticide Use and Genetic Variants Involved in Lipid Metabolism on Prostate Cancer Risk.Journal of cancer epidemiology · 2012Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundPrevious research indicates increased prostate cancer risk for pesticide applicators and pesticide manufacturing workers. Although underlying mechanisms are unknown, evidence suggests a role of oxidative DNA damage.
objectivesBecause base excision repair (BER) is the predominant pathway involved in repairing oxidative damage, we evaluated interactions between 39 pesticides and 394 tag single-nucleotide polymorphisms (SNPs) for 31 BER genes among 776 prostate cancer cases and 1,444 male controls in a nested case-control study of white Agricultural Health Study (AHS) pesticide applicators.
methodsWe used likelihood ratio tests from logistic regression models to determine p-values for interactions between three-level pesticide exposure variables (none/low/high) and SNPs (assuming a dominant model), and the false discovery rate (FDR) multiple comparison adjustment approach.
resultsThe interaction between fonofos and rs1983132 in NEIL3 [nei endonuclease VIII-like 3 (Escherichia coli)], which encodes a glycosylase that can initiate BER, was the most significant overall [interaction p-value (pinteract) = 9.3 × 10-6; FDR-adjusted p-value = 0.01]. Fonofos exposure was associated with a monotonic increase in prostate cancer risk among men with CT/TT genotypes for rs1983132 [odds ratios (95% confidence intervals) for low and high use compared with no use were 1.65 (0.91, 3.01) and 3.25 (1.78, 5.92), respectively], whereas fonofos was not associated with prostate cancer risk among men with the CC genotype. Carbofuran and S-ethyl dipropylthiocarbamate (EPTC) interacted similarly with rs1983132; however, these interactions did not meet an FDR < 0.2.
conclusionsOur significant finding regarding fonofos is consistent with previous AHS findings of increased prostate cancer risk with fonofos exposure among those with a family history of prostate cancer. Although requiring replication, our findings suggest a role of BER genetic variation in pesticide-associated prostate cancer risk.
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